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RESEARCH PAPER / 2024-11-30

Reactive oxygen species in the pathogenesis of sarcopenia.

Hongyang Xu, Jacob L Brown, Shylesh Bhaskaran, Holly Van Remmen

Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, United States. · pubmed

Abstract

One of the most critical factors impacting healthspan in the elderly is the loss of muscle mass and function, clinically referred to as sarcopenia. Muscle atrophy and weakness lead to loss of mobility, increased risk of injury, metabolic changes and loss of independence. Thus, defining the underlying mechanisms of sarcopenia is imperative to enable the development of effective interventions to preserve muscle function and quality in the elderly and improve healthspan. Over the past few decades, understanding the roles of mitochondrial dysfunction and oxidative stress has been a major focus of studies seeking to reveal critical molecular pathways impacted during aging. In this review, we will highlight how oxidative stress might contribute to sarcopenia by discussing the impact of oxidative stress on the loss of innervation and alteration in the neuromuscular junction (NMJ), on muscle mitochondrial function and atrophy pathways, and finally on muscle contractile function.

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper addresses the underlying mechanisms of sarcopenia, which is a significant age-related condition affecting healthspan and quality of life in the elderly. By focusing on oxidative stress and its role in muscle atrophy and function, the research contributes to understanding a root cause of aging-related decline in muscle health. However, as a review, it synthesizes existing knowledge rather than presenting new experimental findings, limiting its overall impact to a solid but not groundbreaking contribution to the field.

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